Blockade of non-opioid analgesia in intruder mice by selective neuronal and non-neuronal benzodiazepine recognition site ligands

Rodgers, R.J.; Randall, J.I.

doi:10.1007/bf02431532

Cited by 21 publications

(2 citation statements)

References 53 publications

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“…3; Miczek et al 1985). In addition to the naloxone-reversible defeat stress-induced analgesia, a modest level of antinociception results from exposure to mild and short attacks by an opponent, and this type of antinociceptive response does not appear to be opioid-mediated since naloxone does not reverse this effect (Rodgers and Randall 1988). …”

Section: Introductionmentioning

confidence: 99%

Gene Expression in Aminergic and Peptidergic Cells During Aggression and Defeat: Relevance to Violence, Depression and Drug Abuse

et al. 2011

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In this review, we examine how experiences in social confrontations alter gene expression in mesocorticolimbic cells. The focus is on the target of attack and threat due to the prominent role of social defeat stress in the study of coping mechanisms and victimization. The initial operational definition of the socially defeated mouse by Ginsburg and Allee (1942) enabled the characterization of key endocrine, cardiovascular, and metabolic events during the initial response to an aggressive opponent and during the ensuing adaptations. Brief episodes of social defeat stress induce an augmented response to stimulant challenge as reflected by increased locomotion and increased extracellular dopamine (DA) in the nucleus accumbens (NAC). Cells in the ventral tegmental area (VTA) that project to the NAC were more active as indicated by increased expression of c-fos and Fos-immunoreactivity and BDNF. Intermittent episodes of social defeat stress result in increased mRNA for MOR in brainstem and limbic structures. These behavioral and neurobiological indices of sensitization persist for several months after the stress experience. The episodically defeated rats also self-administered intravenous cocaine during continuous access for 24 h (“binge”). By contrast, continuous social stress, particularly in the form of social subordination stress, leads to reduced appetite, compromised endocrine activities, and cardiovascular and metabolic abnormalities, and prefer sweets less as index of anhedonia. Cocaine challenges in subordinate rats result in a blunted psychomotor stimulant response and a reduced DA release in NAC. Subordinate rats self-administer cocaine less during continuous access conditions. These contrasting patterns of social stress result from continuous vs. intermittent exposure to social stress, suggesting divergent neuroadaptations for increased vulnerability to cocaine self-administration vs. deteriorated reward mechanisms characteristic of depressive-like profiles.

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Section: Introductionmentioning

confidence: 99%

Gene Expression in Aminergic and Peptidergic Cells During Aggression and Defeat: Relevance to Violence, Depression and Drug Abuse

et al. 2011

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“…A more ethological approach to the study ofbenzodiazepine administration and the blockage of analgesia has been reported by Rodgers and Randall (1987a, 1987b, 1988a, 1988b. These experimenters administered benzodiazepines during resident-intruder sessions and tested for analgesia both before and after such sessions.…”

Section: Methodsmentioning

confidence: 99%

Conditioned fear and analgesia to conspecific odors: Benzodiazepine and 5-HT1A agonists

Hotsenpiller

Williams

1996

Psychobiology

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Neuropharmacological aspects of adaptive pain inhibition in murine “victims” of aggression

Rodgers

1995

Aggr. Behav.

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This review outlines recent research on a subset of physiological responses in murine “victims” or aggression. In a typical resident‐intruder paradigm, the detailed study of intruders has revealed that exposure to conspecific attack (and related stimuli) is associated with two forms of analgesia which appear to be integral components of the murine defensive repertoire. In response to intense/enduring attack, intruder mice display a profound, long‐lasting and opioid‐mediated analgesia. This reaction is highly correlated with defensive immobility and may function to reduce involuntary cues to further attack. In contrast, the inhibition of pain reactivity in mice tested immediately upon the display of defeat is less intense, shorter‐lasting, non‐opioid in nature and may function to facilitate active defenses such as escape. As this form of pain inhibition is also evident in intruders exposed to the scent of an aggressive male conspecific, a possible anticipatory defensive function linked to mechanisms of anxiety has been proposed. This hypothesis is supported by 1) the prevention of defeat analgesia by a range of antianxiety drugs (benzodiazepines, 5‐hydroxytryptamine1A [5‐HT1A] receptor agonists, and 5‐HT3 receptor antagonists) and 2) the effects of social defeat on behavior in the elevated plusmaze model of anxiety. These findings are discussed in relation to coping mechanisms in murine “victims” of aggression. © 1995 Wiley‐Liss, Inc.

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Blockade of non-opioid analgesia in intruder mice by selective neuronal and non-neuronal benzodiazepine recognition site ligands

Cited by 21 publications

References 53 publications

Gene Expression in Aminergic and Peptidergic Cells During Aggression and Defeat: Relevance to Violence, Depression and Drug Abuse

Gene Expression in Aminergic and Peptidergic Cells During Aggression and Defeat: Relevance to Violence, Depression and Drug Abuse

Conditioned fear and analgesia to conspecific odors: Benzodiazepine and 5-HT1A agonists

Neuropharmacological aspects of adaptive pain inhibition in murine “victims” of aggression

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